Journal articles on the topic 'Aortic tissue'

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1

Torfgård, Krishna, Johan Ahlner, Krister L. Axelsson, Björn Norlander, and Åke Bertler. "Tissue levels of glyceryl trinitrate and cGMP after in vivo administration in rat, and the effect of tolerance development." Canadian Journal of Physiology and Pharmacology 69, no. 9 (September 1, 1991): 1257–61. http://dx.doi.org/10.1139/y91-184.

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The present study compares the tissue distribution of glyceryl trinitrate (GTN) in plasma, heart, brain, aortic tissue, and adipose tissue from GTN tolerant and GTN nontolerant rats at various time points. Furthermore, the cGMP levels in brain, heart, and aortic tissue were studied at various time points as well as the concentration–effect relationship for GTN in aorta isolated at different time points after the last exposure to GTN. Concentrations of GTN were found to be higher in all tissues studied as compared with plasma, and the concentrations of GTN were higher in tissues from tolerant rats as compared with nontolerant rats, except for aortic tissue. Concentration–effect curves obtained in vitro showed that aortic smooth muscle was still tolerant 24 h after the last dose of GTN. The cGMP level in brain was significantly increased by 40% 2 h after a single dose of GTN (50 mg/kg) and in aortic tissue by 50% at 15 min and at 2 h after a single dose of GTN (50 mg/kg). There was no effect on cGMP in brain, while an increase was seen in aortic tissue 15 min after the last dose in tolerant animals. No change in cGMP level was seen in heart neither in nontolerant nor in tolerant animals at 15 min and at 2 h. No effect on cGMP levels in brain, heart, and aortic tissue was seen 8, 16, and 24 h after exposure to GTN in either tolerant or nontolerant rats. In conclusion, GTN does not involve the cGMP system in heart, and tolerance development caused a less pronounced GTN-induced cGMP increase in aortic tissue. Furthermore, the cGMP elevation in tissues does not correlate with GTN levels in tissues.Key words: glyceryl trinitrate, cGMP, tolerance, tissue distribution, rat.
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2

Wright, Gary. "Use-dependent decline in rat aorta sensitivity to contraction by potassium." Canadian Journal of Physiology and Pharmacology 69, no. 7 (July 1, 1991): 921–28. http://dx.doi.org/10.1139/y91-140.

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Aortic rings excised from rats at 12 weeks of age showed a decrease in responsiveness during repeated contraction by increasing potassium concentration. By comparison, aortic rings obtained from rats at 22 and 26 weeks exhibited less loss or an increase in responsiveness to high potassium concentration during repeated contraction. The decrease in responsiveness to potassium in aortae of young rats was not due to the extended interval of incubation of the tissue in vitro. Aortic rings incubated without stimulation for 4 h following a reference contraction showed no change in contractile response to potassium. However, the magnitude of loss in responsiveness to potassium did appear to be related to the potassium concentration and the length of time the tissues were exposed to the high potassium solutions. Contraction of the tissue at 60 versus 30 mM KCl or extending the interval in depolarizing solution from 15 to 60 min significantly enhanced the decline in tissue responsiveness to potassium. The interruption of a series of potassium-induced contractions by exposure of the tissue to contractile (serotonin, norepinephrine) or relaxant (acetylcholine, isoproterenol) stimuli had no effect on the loss in responsiveness to potassium. However, injection of the calcium channel agonist, Bay K 8644, into the incubation media restored responsiveness to potassium. Concentration–response curves indicated that both sensitivity and the maximal response to potassium were reduced in aortic rings repeatedly contracted with potassium. Bay K 8644 addition immediately following the control contraction significantly increased sensitivity and the maximal response to potassium compared with the control contraction. After tissues had been repeatedly contracted by potassium, Bay K 8644 restored tissue sensitivity and the maximum response to the control level. The results indicate that aortic tissues of young rats are subject to desensitization to potassium stimulation during repeated exposure in vitro. The restoration of tissue sensitivity by Bay K 8644 suggests that this desensitization centers on decreased effectiveness of the voltage-dependent mechanism for increasing intracellular concentration of free calcium and the activation of the contractile protein.Key words: concentration–response, depolarization, vascular smooth muscle, tension.
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3

Behr-Roussel, Delphine, Diane Gorny, Katell Mevel, Sandrine Compagnie, Patrick Kern, Virgine Sivan, Jacques Bernabé, Martin P. Bedigian, Laurent Alexandre, and François Giuliano. "Erectile dysfunction: an early marker for hypertension? A longitudinal study in spontaneously hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 1 (January 2005): R276—R283. http://dx.doi.org/10.1152/ajpregu.00040.2004.

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Erectile dysfunction (ED) is another manifestation of vascular disease. We evaluated the natural history of ED in the spontaneously hypertensive rat (SHR) and the respective participation of associated pathophysiological modifications, i.e., endothelial dysfunction and tissue remodeling. SHR and their normotensive counterparts [Wistar-Kyoto rats (WKY)] of 6, 12, and 24 wk of age ( n = 12) were used to evaluate erectile function, erectile and aortic tissue reactivity, and remodeling. Erectile responses in SHR are reduced at all ages ( P < 0.001). In both aortic and erectile tissues of SHR and WKY, relaxations to ACh are altered progressively with age, although more markedly in SHR. They are decreased at 12 wk of age in erectile tissue of SHR compared with WKY (maximal relaxation: −19.2 ± 2.8% vs. −28.3 ± 3.9%, P < 0.001) but only at 24 wk of age in aortas (−47.9 ± 6.4% vs. −90.5 ± 2.9%, P < 0.001). Relaxations to sodium nitroprusside are unaltered in aortic rings of both strains but enhanced in erectile tissue of SHR at 12 wk of age. Major modifications in the distribution of collagen I, III, and V in SHR occur in both types of tissue and are detectable sooner in erectile tissue compared with aortic tissue. The onset of ED is detectable before the onset of hypertension in the SHR. Structural and functional alterations, while similar, occur earlier in erectile compared with vascular tissue. If confirmed in humans, ED could be an early warning sign for hypertension, and common therapeutic strategies targeting both ED and hypertension could be investigated.
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4

Zhao, Dong-E., Ruo-Bing Li, Wei-Yong Liu, Gang Wang, Shi-Qiang Yu, Cheng-Wei Zhang, Wen-Sheng Chen, and Geng-Xu Zhou. "Tissue-Engineered Heart Valve on Acellular Aortic Valve Scaffold: In-Vivo Study." Asian Cardiovascular and Thoracic Annals 11, no. 2 (June 2003): 153–56. http://dx.doi.org/10.1177/021849230301100214.

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The feasibility of constructing a tissue-engineered heart valve on an acellular porcine aortic valve leaflet was evaluated. A detergent and enzymatic extraction process was developed to remove the cellular components from porcine aortic valves. The acellular valve leaflets were seeded for 7 days in vitro with cells from canine arterial wall and endothelial cells. The constructs were implanted into the lumens of 6 canine abdominal aortas to assess the reconstruction of the valve leaflets. It was found that all cellular components had been removed from the porcine aortic valves. The valve leaflets were completely reconstructed at the end of the 10th week in vivo. Scanning electron microscopy showed that the valve leaflets were partially covered with endothelial cells. It was concluded that porcine aortic valves can be decellularized by the detergent and enzymatic extraction process and it is feasible to construct a tissue-engineered heart valve in vivo on an acellular valve scaffold.
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5

Li, Yanming, Pingping Ren, Ashley Dawson, Hernan G. Vasquez, Waleed Ageedi, Chen Zhang, Wei Luo, et al. "Single-Cell Transcriptome Analysis Reveals Dynamic Cell Populations and Differential Gene Expression Patterns in Control and Aneurysmal Human Aortic Tissue." Circulation 142, no. 14 (October 6, 2020): 1374–88. http://dx.doi.org/10.1161/circulationaha.120.046528.

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Background: Ascending thoracic aortic aneurysm (ATAA) is caused by the progressive weakening and dilatation of the aortic wall and can lead to aortic dissection, rupture, and other life-threatening complications. To improve our understanding of ATAA pathogenesis, we aimed to comprehensively characterize the cellular composition of the ascending aortic wall and to identify molecular alterations in each cell population of human ATAA tissues. Methods: We performed single-cell RNA sequencing analysis of ascending aortic tissues from 11 study participants, including 8 patients with ATAA (4 women and 4 men) and 3 control subjects (2 women and 1 man). Cells extracted from aortic tissue were analyzed and categorized with single-cell RNA sequencing data to perform cluster identification. ATAA-related changes were then examined by comparing the proportions of each cell type and the gene expression profiles between ATAA and control tissues. We also examined which genes may be critical for ATAA by performing the integrative analysis of our single-cell RNA sequencing data with publicly available data from genome-wide association studies. Results: We identified 11 major cell types in human ascending aortic tissue; the high-resolution reclustering of these cells further divided them into 40 subtypes. Multiple subtypes were observed for smooth muscle cells, macrophages, and T lymphocytes, suggesting that these cells have multiple functional populations in the aortic wall. In general, ATAA tissues had fewer nonimmune cells and more immune cells, especially T lymphocytes, than control tissues did. Differential gene expression data suggested the presence of extensive mitochondrial dysfunction in ATAA tissues. In addition, integrative analysis of our single-cell RNA sequencing data with public genome-wide association study data and promoter capture Hi-C data suggested that the erythroblast transformation-specific related gene( ERG ) exerts an important role in maintaining normal aortic wall function. Conclusions: Our study provides a comprehensive evaluation of the cellular composition of the ascending aortic wall and reveals how the gene expression landscape is altered in human ATAA tissue. The information from this study makes important contributions to our understanding of ATAA formation and progression.
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6

Chowdhury, Ujjwal Kumar, Lakshmi Kumari Sankhyan, Sheil Avneesh, Ruma Ray, Mani Kalaivani, Suruchi Hasija, and Abhinavsingh Chauhan. "Histologic Abnormalities of the Ascending Aorta: Effects on Aortic Remodeling after Intracardiac Repair of Tetralogy of Fallot." Texas Heart Institute Journal 47, no. 2 (April 1, 2020): 86–95. http://dx.doi.org/10.14503/thij-17-6279.

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We evaluated aortic tissue specimens from patients undergoing tetralogy of Fallot repair, to determine whether histologic abnormalities affect postsurgical aortic remodeling and other patient-related variables. Using light microscopy, we studied full-thickness aortic wall tissue operatively excised from 118 consecutive patients undergoing intracardiac repair of tetralogy of Fallot. We performed multiple linear regression analysis to identify independent predictors of change in aortic root dimensions, which we measured with echocardiography after repair and every 3 months thereafter. Thirty histologically normal specimens were used as controls. Elastic fiber fragmentation was found in 74.6% of the abnormal specimens, mucoid extracellular matrix accumulation in 49.2%, smooth muscle cell nuclei loss in 39%, smooth muscle cell disorganization in 28.8%, and medial fibrosis in 52.5%. At a mean follow-up time of 83.55 ± 42.08 months, mean aortic sinotubular diameter decreased from 28.79 ± 9.15 to 27.16 ± 8.52 mm/m2 (r =–0.43; P &lt;0.001). Aortic sinotubular diameter decreased by 0.6 mm/m2 among females (β =0.6, SE=0.31; P =0.05) and by 0.88 mm/m2 in patients who had elastic fiber fragmentation or loss (β =0.88, SE=0.38; P =0.02). In bivariate and multiple linear regression analysis, duration of follow-up emerged as an independent predictor of aortic remodeling. The aortic histopathologic changes in our patients had an independent negative impact on the degree of aortic remodeling after surgery. We observed the most improved aortic sinotubular diameter in patients who had either histologically normal aortas or aortas with elastic fragmentation.
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7

Harky, Amer, Rizwan Iqbal, Vincenzo Giordano, and Ahmed Al-Adhami. "Aortic endovascular stenting in patients with systemic connective tissue disorders: does the prohibitive dogma still stand tall?" Journal of International Medical Research 48, no. 2 (July 29, 2019): 030006051986396. http://dx.doi.org/10.1177/0300060519863963.

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Endovascular repair of thoracic aortic diseases can provide satisfactory outcomes in elective and certain emergency cases involving the descending thoracic and aortic arch. However, open repair remains the gold standard method of aortic root pathologies and certain aortic arch pathologies, such as extended dissection. Nevertheless, the use of endovascular stenting in patients with connective tissue disorders has not been fully explored because the aortic tissues are fragile and the likelihood of keeping the stent in place is low because of its progressive dilatation and subsequent requirement for open repair at a later stage when the stent graft fails. Our brief review focuses on current evidence of the use of stents in patients with connective tissue disorders and whether such practice can be expanded further.
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8

Alakhtar, Ali, Alexander Emmott, Cornelius Hart, Rosaire Mongrain, Richard L. Leask, and Kevin Lachapelle. "3D printed ascending aortic simulators with physiological fidelity for surgical simulation." BMJ Simulation and Technology Enhanced Learning 7, no. 6 (June 21, 2021): 536–42. http://dx.doi.org/10.1136/bmjstel-2021-000868.

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IntroductionThree-dimensional (3D) printed multimaterial ascending aortic simulators were created to evaluate the ability of polyjet technology to replicate the distensibility of human aortic tissue when perfused at physiological pressures.MethodsSimulators were developed by computer-aided design and 3D printed with a Connex3 Objet500 printer. Two geometries were compared (straight tube and idealised aortic aneurysm) with two different material variants (TangoPlus pure elastic and TangoPlus with VeroWhite embedded fibres). Under physiological pressure, β Stiffness Index was calculated comparing stiffness between our simulators and human ascending aortas. The simulators’ material properties were verified by tensile testing to measure the stiffness and energy loss of the printed geometries and composition.ResultsThe simulators’ geometry had no effect on measured β Stiffness Index (p>0.05); however, β Stiffness Index increased significantly in both geometries with the addition of embedded fibres (p<0.001). The simulators with rigid embedded fibres were significantly stiffer than average patient values (41.8±17.0, p<0.001); however, exhibited values that overlapped with the top quartile range of human tissue data suggesting embedding fibres can help replicate pathological human aortic tissue. Biaxial tensile testing showed that fiber-embedded models had significantly higher stiffness and energy loss as compared with models with only elastic material for both tubular and aneurysmal geometries (stiffness: p<0.001; energy loss: p<0.001). The geometry of the aortic simulator did not statistically affect the tensile tested stiffness or energy loss (stiffness: p=0.221; energy loss: p=0.713).ConclusionWe developed dynamic ultrasound-compatible aortic simulators capable of reproducing distensibility of real aortas under physiological pressures. Using 3D printed composites, we are able to tune the stiffness of our simulators which allows us to better represent the stiffness variation seen in human tissue. These models are a step towards achieving better simulator fidelity and have the potential to be effective tools for surgical training.
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9

Pedroza, Albert J., Yasushi Tashima, Rohan Shad, Paul Cheng, Robert Wirka, Samantha Churovich, Ken Nakamura, et al. "Single-Cell Transcriptomic Profiling of Vascular Smooth Muscle Cell Phenotype Modulation in Marfan Syndrome Aortic Aneurysm." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 9 (September 2020): 2195–211. http://dx.doi.org/10.1161/atvbaha.120.314670.

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Objective: To delineate temporal and spatial dynamics of vascular smooth muscle cell (SMC) transcriptomic changes during aortic aneurysm development in Marfan syndrome (MFS). Approach and Results: We performed single-cell RNA sequencing to study aortic root/ascending aneurysm tissue from Fbn1 C1041G/ + (MFS) mice and healthy controls, identifying all aortic cell types. A distinct cluster of transcriptomically modulated SMCs (modSMCs) was identified in adult Fbn1 C1041G/ + mouse aortic aneurysm tissue only. Comparison with atherosclerotic aortic data (ApoE −/− mice) revealed similar patterns of SMC modulation but identified an MFS-specific gene signature, including plasminogen activator inhibitor-1 ( Serpine1 ) and Kruppel-like factor 4 ( Klf4 ). We identified 481 differentially expressed genes between modSMC and SMC subsets; functional annotation highlighted extracellular matrix modulation, collagen synthesis, adhesion, and proliferation. Pseudotime trajectory analysis of Fbn1 C1041G/ + SMC/modSMC transcriptomes identified genes activated differentially throughout the course of phenotype modulation. While modSMCs were not present in young Fbn1 C1041G/ + mouse aortas despite small aortic aneurysm, multiple early modSMCs marker genes were enriched, suggesting activation of phenotype modulation. modSMCs were not found in nondilated adult Fbn1 C1041G/ + descending thoracic aortas. Single-cell RNA sequencing from human MFS aortic root aneurysm tissue confirmed analogous SMC modulation in clinical disease. Enhanced expression of TGF-β (transforming growth factor beta)-responsive genes correlated with SMC modulation in mouse and human data sets. Conclusions: Dynamic SMC phenotype modulation promotes extracellular matrix substrate modulation and aortic aneurysm progression in MFS. We characterize the disease-specific signature of modSMCs and provide temporal, transcriptomic context to the current understanding of the role TGF-β plays in MFS aortopathy. Collectively, single-cell RNA sequencing implicates TGF-β signaling and Klf4 overexpression as potential upstream drivers of SMC modulation.
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10

Tascini, Carlo, Antonello Di Paolo, Roberta Poletti, Sarah Flammini, Michele Emdin, Ilaria Ciullo, Enrico Tagliaferri, Annette Moter, and Francesco Menichetti. "Daptomycin Concentrations in Valve Tissue and Vegetation in Patients with Bacterial Endocarditis." Antimicrobial Agents and Chemotherapy 57, no. 1 (October 22, 2012): 601–2. http://dx.doi.org/10.1128/aac.01608-12.

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ABSTRACTIn a patient with mitral-aortic native-valveStreptococcus oralisendocarditis, daptomycin concentrations in aortic and mitral valves were 8.6 and 30.8 μg/g, respectively, and 26 μg/g in the mitral vegetation. In the case of porcine-aortic-valveStaphylococcus epidermidisendocarditis, the daptomycin concentrations were 53.1 μg/g in the valve and 18.1 μg/g in perivalvular tissues. Daptomycin achieved apparently adequate tissue concentrations.S. epidermidiswas eradicated, whereasStreptococcus oralispersisted, and its daptomycin MIC displayed a 4-fold increase.
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11

Rodríguez-Carrio, Javier, Jes S. Lindholt, Marina Canyelles, Diego Martínez-López, Mireia Tondo, Luis M. Blanco-Colio, Jean-Baptiste Michel, Joan Carles Escolà-Gil, Ana Suárez, and José Luis Martín-Ventura. "IgG Anti-High Density Lipoprotein Antibodies Are Elevated in Abdominal Aortic Aneurysm and Associated with Lipid Profile and Clinical Features." Journal of Clinical Medicine 9, no. 1 (December 26, 2019): 67. http://dx.doi.org/10.3390/jcm9010067.

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High-density lipoproteins cholesterol (HDLc) levels are decreased in abdominal aortic aneurysm (AAA), which is hallmarked by autoimmunity and lipid aortic deposits. To investigate whether IgG anti-HDL antibodies were present in AAA and their potential association with clinical features, IgG anti-HDL and total IgG along with HDLc plasma levels were measured in 488 AAA patients and 184 controls from the Viborg Vascular (VIVA) study, and in tissue-conditioned media from AAA intraluminal thrombus and media layer samples compared to control aortas. Higher IgG anti-HDL levels were found in AAA compared to controls, even after correcting for total IgG, and after adjusting for potential confounders. IgG anti-HDL levels were correlated with aortic diameter in univariate and adjusted multivariate analyses. IgG anti-HDL antibodies were negatively associated with HDLc levels before and after correcting for potential confounders. Increased anti-HDL antibodies were identified in tissue-conditioned media from AAA samples compared to healthy aortas, with higher levels being observed in the media layer. In conclusion, increased IgG anti-HDL levels (both in plasma and in tissue) are linked to AAA, associated with aortic diameter and HDLc levels. These data suggest a potential immune response against HDL in AAA and support an emerging role of anti-HDL antibodies in AAA.
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12

Forneris, Arianna, Miriam Nightingale, Alina Ismaguilova, Taisiya Sigaeva, Louise Neave, Amy Bromley, Randy D. Moore, and Elena S. Di Martino. "Heterogeneity of Ex Vivo and In Vivo Properties along the Length of the Abdominal Aortic Aneurysm." Applied Sciences 11, no. 8 (April 13, 2021): 3485. http://dx.doi.org/10.3390/app11083485.

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The current clinical guidelines for the management of aortic abdominal aneurysms (AAAs) overlook the structural and mechanical heterogeneity of the aortic tissue and its role in the regional weakening that drives disease progression. This study is a comprehensive investigation of the structural and biomechanical heterogeneity of AAA tissue along the length and circumference of the aorta, by means of regional ex vivo and in vivo properties. Biaxial testing and histological analysis were performed on ex vivo human aortic specimens systematically collected during open repair surgery. Wall-shear stress and three-dimensional principal strain analysis were performed to allow for in vivo regional characterization of individual aortas. A marked effect of position along the aortic length was observed in both ex vivo and in vivo properties, with the central regions corresponding to the aneurysmal sac being significantly different from the adjacent regions. The heterogeneity along the circumference of the aorta was reflected in the ex vivo biaxial response at low strains and histological properties. Present findings uniquely show the importance of regional characterization for aortic assessment and the need to correlate heterogeneity at the tissue level with non-invasive measurements aimed at improving clinical outcomes.
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13

Briffa, Norman Paul. "Results of mechanical versus tissue AVR: caution in young patients with tissue AVR." Heart 105, Suppl 2 (March 2019): s34—s37. http://dx.doi.org/10.1136/heartjnl-2018-313516.

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The first aortic valve prosthesis, implanted more than 50 years ago, was a mechanical prosthesis (ball-and-cage design). Over the ensuing decades, tissue prostheses and new mechanical designs were introduced to mitigate the need for anticoagulation with its associated side effects. Tissue and mechanical heart valve prostheses were compared in two head-to-head randomised control trials. Both of these confirmed that mechanical prostheses were durable but patients suffered anticoagulant-related bleeds. Patients who received a tissue prosthesis were more likely to suffer prosthetic dysfunction and require reoperation. This trend was stronger in younger patients. Since the publication of those two trials, several large retrospective studies using data from meta-analyses of published papers or registries have failed to show a survival advantage of either prostheses when implanted in the aortic position in younger patients. This equipoise has been reflected in the heart valve disease guidelines published by European and US societies. In recent years, the primacy of patient choice, the rapid increase in life expectancy of populations, the increased incidence of atrial fibrillation with requirement for anticoagulation, the advent of transcatheter techniques to treat degenerating tissue valves as well as advances in anticoagulant therapy and in new tissue and to a lesser extent mechanical prosthetic design continue to influence choice of aortic valve prosthesis in younger patients undergoing aortic valve replacement.
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14

Doraiswamy, Anand, and Roger J. Narayan. "Vascular tissue engineering by computer-aided laser micromachining." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 368, no. 1917 (April 28, 2010): 1891–912. http://dx.doi.org/10.1098/rsta.2010.0004.

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Many conventional technologies for fabricating tissue engineering scaffolds are not suitable for fabricating scaffolds with patient-specific attributes. For example, many conventional technologies for fabricating tissue engineering scaffolds do not provide control over overall scaffold geometry or over cell position within the scaffold. In this study, the use of computer-aided laser micromachining to create scaffolds for vascular tissue networks was investigated. Computer-aided laser micromachining was used to construct patterned surfaces in agarose or in silicon, which were used for differential adherence and growth of cells into vascular tissue networks. Concentric three-ring structures were fabricated on agarose hydrogel substrates, in which the inner ring contained human aortic endothelial cells, the middle ring contained HA587 human elastin and the outer ring contained human aortic vascular smooth muscle cells. Basement membrane matrix containing vascular endothelial growth factor and heparin was to promote proliferation of human aortic endothelial cells within the vascular tissue networks. Computer-aided laser micromachining provides a unique approach to fabricate small-diameter blood vessels for bypass surgery as well as other artificial tissues with complex geometries.
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15

Donadille, Bruno, Alexander Valent, Kisaki Amemiya, Nicolas Rive le Gouard, Laurence Iserin, Paul Achouh, Tatiana Lecot-Connan, Patrick Bruneval, Jean-Pierre Siffroi, and Sophie Christin-Maitre. "Aortic Tissue Analysis in Turner Syndrome." Journal of the American College of Cardiology 80, no. 13 (September 2022): 1284–85. http://dx.doi.org/10.1016/j.jacc.2022.07.017.

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16

Bertelsen, Sv, and C. E. Jensen. "HISTOCHEMICAL STUDIES ON HUMAN AORTIC TISSUE." Acta Pathologica Microbiologica Scandinavica 48, no. 4 (August 15, 2009): 305–15. http://dx.doi.org/10.1111/j.1699-0463.1960.tb04770.x.

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17

Willems, Tineke P., Johanna J. M. Takkenberg, Ewout W. Steyerberg, Veronica E. Kleyburg-Linkers, Jos R. T. C. Roelandt, Egbert Bos, and Lex A. van Herwerden. "Human Tissue Valves in Aortic Position." Circulation 103, no. 11 (March 20, 2001): 1515–21. http://dx.doi.org/10.1161/01.cir.103.11.1515.

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18

Spieker, Claus, Walter Zidek, Dirk B. von Bassewitz, Dieter Heck, and Hans Vetter. "Analysis of Ca2+ in aortic tissue." Journal of Hypertension 6, no. 4 (December 1988): S192–195. http://dx.doi.org/10.1097/00004872-198812040-00057.

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19

Fraisse, A., E. Le Bret, T. Abdel Massih, A. Batisse, F. Laborde, D. Sidi, and D. Bonnet. "Intra-aortic extension of ductal tissue." Journal of Thoracic and Cardiovascular Surgery 123, no. 3 (March 2002): 568–69. http://dx.doi.org/10.1067/mtc.2002.121759.

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20

BORST, H., J. LAAS, and B. BUHNER. "Efficient tissue gluing in aortic dissection." European Journal of Cardio-Thoracic Surgery 8, no. 3 (1994): 160–61. http://dx.doi.org/10.1016/1010-7940(94)90176-7.

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21

Di Bello, Vitantonio, Cuono Cucco, Cristina Giannini, and Maria Grazia Delle Donne. "Myocardial Tissue Characterization and Aortic Stenosis." Journal of the American Society of Echocardiography 23, no. 10 (October 2010): 1067–70. http://dx.doi.org/10.1016/j.echo.2010.08.025.

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22

Zimmermann, W. "Tissue engineering of aortic heart valves." Cardiovascular Research 60, no. 3 (December 1, 2003): 460–62. http://dx.doi.org/10.1016/j.cardiores.2003.10.007.

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23

Muramatsu, Ikunobu, Adebayo Laniyonu, Graham J. Moore, and Morley D. Hollenberg. "Vascular actions of thrombin receptor peptide." Canadian Journal of Physiology and Pharmacology 70, no. 7 (July 1, 1992): 996–1003. http://dx.doi.org/10.1139/y92-137.

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We have examined the action of the thrombin receptor-derived polypeptide, S42FLLRNPNDKYEPF55 (TRP42–55), in rat and guinea pig aortic rings and helical arterial strips, and we have compared the actions of the peptide with those of thrombin. In rat preparations, both TRP 42–55 and thrombin caused a concentration-dependent endothelium-dependent relaxation that was blocked by Nω-nitro-L-arginine methyl ester; the relaxation response of the intact rat aortic strip preparation to concentrations of the peptide in the range 30–60 μg/mL (17–34 μM) was equivalent to the response to 0.03–0.1 U/mL of thrombin (about 0.3–0.9 nM), yielding a potency ratio (TRP 42–55:thrombin) of about 38 000: 1. In contrast with the complete desensitization of thrombin-treated rat aortic preparations to a second administration of the enzyme, the rat aortic tissue was not desensitized by repeated exposures to TRP 42–55 and remained responsive to the peptide even after treatment of the tissue by thrombin. In contrast with the rat aortic tissue, in either intact or endothelium-free guinea pig aortic preparations both TRP 42–55 and thrombin caused a concentration-dependent endothelium-independent contraction. The contractile action of 60 μg/mL of receptor peptide (34 μM) in guinea pig aortic strip preparations was equivalent to the contractile action of 0.1–0.3 U/mL thrombin (0.9–3 nM), yielding a potency ratio of about 17 000: 1. In guinea pig aortic preparations with an intact endothelium that were precontracted with noradrenaline, neither thrombin nor TRP 42–55 caused relaxation, whereas substance P did so. As with the rat aortic preparation, thrombin treatment of the guinea pig aorta rendered the tissue refractory to a second exposure to the enzyme, whereas treatment with the receptor peptide did not desensitize the tissue to a subsequent exposure to thrombin. Nonetheless, as opposed to the rat aortic preparation, wherein repeated exposure to the peptide yielded a constant response, repeat doses of TRP 42–55 caused a modest desensitization of its contractile action in the guinea pig aortic strip preparation. None of the effects of TRP 42–55 were affected by the thrombin inhibitor hirudin, which blocked the action of thrombin in both the rat and guinea pig aortic preparations. We conclude that the distinct effects of TRP 42–55 in both rat and guinea pig aortic tissue, which mimic the actions of thrombin in both preparations, are due to the presence of a thrombin receptor in these tissues, akin to the one previously characterized in platelet tissue. Further, the data indicating different TRP 42–55:thrombin potency ratios and different desensitizing properties in the rat and guinea pig aortic tissue support the notion that there may be distinct thrombin receptor signal transduction systems that regulate vascular contractility either directly by acting on smooth muscle elements or indirectly via an action on endothelial cells.Key words: thrombin, thrombin receptor, vasoconstriction, vasorelaxation, aorta, endothelium.
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24

Martin, Emil, Eva Golunski, Susan T. Laing, Anthony L. Estrera, and Iraida G. Sharina. "Alternative splicing impairs soluble guanylyl cyclase function in aortic aneurysm." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 11 (December 1, 2014): H1565—H1575. http://dx.doi.org/10.1152/ajpheart.00222.2014.

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Nitric oxide (NO) receptor soluble guanylyl cyclase (sGC) is a key regulator of several important vascular functions and is important for maintaining cardiovascular homeostasis and vascular plasticity. Diminished sGC expression and function contributes to pathogenesis of several cardiovascular diseases. However, the processes that control sGC expression in vascular tissue remain poorly understood. Previous work in animal and cell models revealed the complexity of alternative splicing of sGC genes and demonstrated its importance in modulation of sGC function. The aim of this study was to examine the role of alternative splicing of α1 and β1 sGC in healthy and diseased human vascular tissue. Our study found a variety of α1 and β1 sGC splice forms expressed in human aorta. Their composition and abundance were different between samples of aortic tissue removed during surgical repair of aortic aneurysm and samples of aortas without aneurysm. Aortas with aneurysm demonstrated decreased sGC activity, which correlated with increased expression of dysfunctional sGC splice variants. In addition, the expression of 55-kDa oxidation-resistant α1 isoform B sGC (α1-IsoB) was significantly lower in aortic samples with aneurysm. The α1-IsoB splice variant was demonstrated to support sGC activity in aortic lysates. Together, our results suggest that alternative splicing contributes to diminished sGC function in vascular dysfunction. Precise understanding of sGC splicing regulation could help to design new therapeutic interventions and to personalize sGC-targeting therapies in treatments of vascular disease.
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Sugita, Shukei, and Takeo Matsumoto. "OS18-9 Microscopic Deformation of Porcine Thoracic Aortas until Failure during Biaxial Stretch as a Model of Aortic Rupture(Cell and Tissue mechanics 3,OS18 Cell and tissue mechanics,BIOMECHANICS)." Abstracts of ATEM : International Conference on Advanced Technology in Experimental Mechanics : Asian Conference on Experimental Mechanics 2015.14 (2015): 243. http://dx.doi.org/10.1299/jsmeatem.2015.14.243.

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Kossar, Alexander P., Wanda Anselmo, Juan B. Grau, Yichuan Liu, Aeron Small, Samuel L. Carter, Lisa Salvador, et al. "Circulating and tissue matricellular RNA and protein expression in calcific aortic valve disease." Physiological Genomics 52, no. 4 (April 1, 2020): 191–99. http://dx.doi.org/10.1152/physiolgenomics.00104.2019.

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Aortic valve sclerosis is a highly prevalent, poorly characterized asymptomatic manifestation of calcific aortic valve disease and may represent a therapeutic target for disease mitigation. Human aortic valve cusps and blood were obtained from 333 patients undergoing cardiac surgery ( n = 236 for severe aortic stenosis, n = 35 for asymptomatic aortic valve sclerosis, n = 62 for no valvular disease), and a multiplex assay was used to evaluate protein expression across the spectrum of calcific aortic valve disease. A subset of six valvular tissue samples ( n = 3 for asymptomatic aortic valve sclerosis, n = 3 for severe aortic stenosis) was used to create RNA sequencing profiles, which were subsequently organized into clinically relevant gene modules. RNA sequencing identified 182 protein-encoding, differentially expressed genes in aortic valve sclerosis vs. aortic stenosis; 85% and 89% of expressed genes overlapped in aortic stenosis and aortic valve sclerosis, respectively, which decreased to 55% and 84% when we targeted highly expressed genes. Bioinformatic analyses identified six differentially expressed genes encoding key extracellular matrix regulators: TBHS2, SPARC, COL1A2, COL1A1, SPP1, and CTGF. Differential expression of key circulating biomarkers of extracellular matrix reorganization was observed in control vs. aortic valve sclerosis (osteopontin), control vs. aortic stenosis (osteoprotegerin), and aortic valve sclerosis vs. aortic stenosis groups (MMP-2), which corresponded to valvular mRNA expression. We demonstrate distinct mRNA and protein expression underlying aortic valve sclerosis and aortic stenosis. We anticipate that extracellular matrix regulators can serve as circulating biomarkers of early calcific aortic valve disease and as novel targets for early disease mitigation, pending prospective clinical investigations.
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Holt, Margrethe, Bjørn E. Seim, Jonas Øgaard, Maria B. Olsen, Per R. Woldbæk, John-Peder Escobar Kvitting, Pål Aukrust, et al. "Selective and marked decrease of complement receptor C5aR2 in human thoracic aortic aneurysms: a dysregulation with potential inflammatory effects." Open Heart 6, no. 2 (November 2019): e001098. http://dx.doi.org/10.1136/openhrt-2019-001098.

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ObjectiveThe aetiology of thoracic aortic aneurysm (TAA) is largely unknown, but inflammation is likely to play a central role in the pathogenesis. In this present study, we aim to investigate the complement receptors in TAA.MethodsAortic tissue and blood from 31 patients with non-syndromic TAA undergoing thoracic aortic repair surgery were collected. Aortic tissue and blood from 36 patients with atherosclerosis undergoing coronary artery bypass surgery or aortic valve replacement were collected and served as control material. The expression of the complement anaphylatoxin receptors C3aR1, C5aR1 and C5aR2 in aortic tissue were examined by quantitative RT-PCR and C5aR2 protein by immunohistochemistry. Colocalisation of C5aR2 to different cell types was analysed by immunofluorescence. Complement activation products C3bc and sC5b-9 were measured in plasma.ResultsCompared with controls, TAA patients had substantial (73%) downregulated gene expression of C5aR2 as seen both at the mRNA (p=0.005) level and protein (p=0.03) level. In contrast, there were no differences in the expression of C3aR1 and C5aR1 between the two groups. Immunofluorescence examination showed that C5aR2 was colocalised to macrophages and T cells in the aortic media. There were no differences in the degree of systemic complement activation between the two groups.ConclusionOur findings suggest downregulation of the C5aR2, regarded to act mainly anti-inflammatory, in electively operated TAA as compared with non-aneurysmatic aortas of patients with aortic stenosis and/or coronary artery disease. This may tip the balance towards a relative increase in the inflammatory responses induced by C5aR1 and thus enhance the inflammatory processes in TAA.
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Wright, G. L., M. E. Rogerson, and W. D. McCumbee. "Stimulation of aortic tissue calcium uptake by an extract of spontaneously hypertensive rats erythrocytes possessing hypertensive properties." Canadian Journal of Physiology and Pharmacology 64, no. 12 (December 1, 1986): 1515–20. http://dx.doi.org/10.1139/y86-255.

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In earlier reports we have described the isolation of a fraction from the erythrocytes of spontaneously hypertensive rats that produced hypertension when administered to normotensive rats. In addition, it was found that the fraction stimulated the uptake of "lanthanum-resistant" calcium by aortic rings excised from normotensive rats. In these studies we have found that the fraction causes a greater increase in the in vitro uptake of calcium by aortic tissue than that produced by depolarization of the tissue with high K+ or the receptor-mediated influx of calcium induced with norepinephrine. The hypertensive fraction appeared to be more effective in promoting increased calcium uptake in rabbit than in rat aortic tissue, suggesting that significant differences in tissue sensitivity to the active compound(s) may exist between species. In addition, we obtained evidence indicating that the tissue sensitivity to the action of the hypertensive fraction was greater in aortae from spontaneously hypertensive rats than from those of normotensive animals. Attempts to block the action of the hypertensive fraction with verapamil, nifedipine, and sodium nitroprusside had no significant effect on the elevation in tissue calcium. It was found, however, that the action of the hypertensive fraction was temperature dependent with reduced activity at lower temperatures. The data suggest that a compound(s) is present in the erythrocytes of rats that may have a marked effect on vascular tissue metabolism of calcium.
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Nonaka, Risa, Takafumi Iesaki, Aurelien Kerever, and Eri Arikawa-Hirasawa. "Increased Risk of Aortic Dissection with Perlecan Deficiency." International Journal of Molecular Sciences 23, no. 1 (December 28, 2021): 315. http://dx.doi.org/10.3390/ijms23010315.

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Perlecan (HSPG2), a basement membrane-type heparan sulfate proteoglycan, has been implicated in the development of aortic tissue. However, its role in the development and maintenance of the aortic wall remains unknown. Perlecan-deficient mice (Hspg2−/−-Tg: Perl KO) have been found to show a high frequency (15–35%) of aortic dissection (AD). Herein, an analysis of the aortic wall of Perl KO mice revealed that perlecan deficiency caused thinner and partially torn elastic lamina. Compared to the control aortic tissue, perlecan-deficient aortic tissue showed a significant decrease in desmosine content and an increase in soluble tropoelastin levels, implying the presence of immature elastic fibers in Perl KO mice. Furthermore, the reduced expression of the smooth muscle cell contractile proteins actin and myosin in perlecan-deficient aortic tissue may explain the risk of AD. This study showed that a deficiency in perlecan, which is localized along the elastic lamina and at the interface between elastin and fibrillin-1, increased the risk of AD, largely due to the immaturity of extracellular matrix in the aortic tissue. Overall, we proposed a new model of AD that considers the deficiency of extracellular molecule perlecan as a risk factor.
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Matt, P., and F. Eckstein. "eComment: Stabilizing aortic tissue after aortic root surgery in Marfan syndrome." Interactive CardioVascular and Thoracic Surgery 7, no. 6 (December 1, 2008): 1166. http://dx.doi.org/10.1510/icvts.2008.183103a.

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DOSSCHE, K., A. DELARIVIERE, W. MORSHUIS, M. SCHEPENS, and J. ERNST. "Aortic root replacement with human tissue valves in aortic valve endocarditis." European Journal of Cardio-Thoracic Surgery 12, no. 1 (July 1997): 47–55. http://dx.doi.org/10.1016/s1010-7940(97)00145-0.

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Meng, YH, C. Tian, L. Liu, L. Wang, and Q. Chang. "Elevated expression of connective tissue growth factor, osteopontin and increased collagen content in human ascending thoracic aortic aneurysms." Vascular 22, no. 1 (May 13, 2013): 20–27. http://dx.doi.org/10.1177/1708538112472282.

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Little is known about the molecular mechanisms of ascending thoracic aortic aneurysms (ATAAs). Abnormal extracellular matrix changes and variations of vascular smooth muscle cells (VSMCs) have been implicated in abdominal aortic aneurysm formation. Our objective was to investigate the alterations of collagen, stimulators of collagen synthesis and synthetic VSMCs in patients with ATAA. Surgical samples from ATAA were taken from 20 patients, and 18 control aortas were obtained during coronary artery bypass surgery. All aortic wall specimens were fixed for histology and immunohistochemistry for collagen, connective tissue growth factor (CTGF) and osteopontin. Realtime polymerase chain reaction was used to determine their mRNA expression. Histology and semi-quantitative analysis demonstrated that protein levels of collagen, CTGF and osteopontin significantly increased by 1.9-, 1.4- and 2.2-fold, respectively ( P < 0.01 for all) in the ATAA group than in the control group. Similar results were shown in mRNA levels of type Iα1and IIIα1 collagen, CTGF and osteopontin. The protein levels of CTGF and osteopontin were positively correlated with aortic diameter ( r = 0.67, r = 0.73; P < 0.01 for both). In conclusion, overexpression of aortic CTGF and synthetic VSMCs marker (osteopontin), which is likely to be responsible for elevated aortic collagen content, may provide a potential mechanism for aneurysmal enlargement.
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Bertelsen, Sv. "ADRENALIN-INDUCED ALTERATIONS IN AORTIC TISSUE OF RABBITS COMPARED WITH CHANGES IN HUMAN AORTIC TISSUE WITH AGE." Acta Pathologica Microbiologica Scandinavica 53, no. 4 (August 18, 2009): 335–44. http://dx.doi.org/10.1111/j.1699-0463.1961.tb00417.x.

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34

Lubec, Barbara, Klaus Arbeiter, Harald Hoeger, and Gert Lubec. "Increased Cyclin Dependent Kinase in Aortic Tissue of Rats Fed Homocysteine." Thrombosis and Haemostasis 75, no. 04 (1996): 542–45. http://dx.doi.org/10.1055/s-0038-1650317.

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Summary Background. Hyperhomocyst(e)inemia is strongly associated with occlusive arterial disease. Several mechanisms for the development of vascular lesions have been described. A direct effect of homocysteine on proliferation of smooth muscle cells and collagen expression was proposed recently. These observations led us to examine the effect of homocysteine on cyclin dependent kinase, the starter of mitosis and reflecting proliferation. Methods and results. Thirty Him: OF A rats were divided into three groups. Ten animals were fed for a period of six weeks 50 mg/kg body wt per day homocysteine, ten the same dose of homocysteic acid and ten remained untreated controls. At the end of the experiment we determined aortic cyclin dependent kinase, phosphokinases A and C, aortic homocyst(e)ine and aortic hydroxyproline. Aortic cyclin dependent kinase was significantly (p = 0.0001) elevated in the homocysteine treated group (mean 120 ± 15) compared with the homocysteic acid treated group (mean 71 ± 11) or the untreated group (mean 72 ± 10 fmol/mg aortic tissue). Aortic homocyst(e)ine was significantly higher in homocysteine treated animals (p = 0.0002) strongly correlating with cyclin dependent kinase (r squared = 0.85, p = 0.0001) and with aortic hydroxyproline (r squared = 0.66, p = 0.0001), which in turn was significantly (p = 0.0001) increased in the homocysteine treated group. Phosphokinases A and C determined to rule out nonspecific effects on kinases were not increased by administered homocysteine. Conclusions. Our findings indicate that homocysteine stimulates aortic cyclin dependent kinase with the possible consequence of proliferation of aortic cells. Aortic collagen accumulation could be explained by either the homocysteine-effect on collagen synthesis described in literature, or secondarily, by increased proliferation of collagen producing aortic cells.
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Luk, Adriana, Tirone E. David, and Jagdish Butany. "Complications of Bioglue postsurgery for aortic dissections and aortic valve replacement." Journal of Clinical Pathology 65, no. 11 (August 7, 2012): 1008–12. http://dx.doi.org/10.1136/jclinpath-2012-200809.

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AimsBioglue is an adhesive used during cardiovascular surgery to improve hemostasis perioperatively and to strengthen and reinforce vascular anastomoses. It has also been used to ‘seal’ the false lumen in patients presenting with acute aortic dissections. Herein, we examine the complications of Bioglue, which may lead to redo sternotomy in selected patients.MethodsA review of pathology records at our institution from 2002 to 2010 found 4 cases of excised aortic tissue and/or aortic valves with previous Bioglue® use at initial operation. Excised tissues and valves were examined, looking for the presence of Bioglue®, inflammatory cells (acute, chronic, macrophage and giant cells) and micro-organisms. Patient demographics were also reviewed and recorded.ResultsWe identified four cases of Bioglue use found at redo surgery, after the formation of pseudoaneurysm (n=3) and aortic stenosis (n=1). Mean interval to redo surgery was 2.28 + 0.32 years (range 2-2.6 years). Pseudoaneurysm formation was thought to be caused by an inflammatory reaction to the Bioglue® itself in two cases, while one case found no such reaction. One patient with previous aortic valve replacement had large annular abscesses filled with necrotic debris surrounding the prosthesis and pannus found on the sewing cuff, comprised of Bioglue® itself.ConclusionsThe mechanisms leading to these complications include mechanical strain, inflammation and tissue necrosis. The judicious use of Bioglue® when clinically indicated, and close follow-up of these patients with serial imaging, remain an integral part of avoiding future complications.
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Chan, Crystal Yin Tung, and Stephen Wing Keung Cheng. "Elevated homocysteine in human abdominal aortic aneurysmal tissues." Vascular Medicine 22, no. 5 (July 14, 2017): 370–77. http://dx.doi.org/10.1177/1358863x17718260.

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An abnormally high level of homocysteine (Hcy) has been consistently observed in the blood of abdominal aortic aneurysm (AAA) patients. However, the expression of Hcy in human AAA tissues has not been investigated. In this study, the expression of Hcy in aneurysmal tissues from AAA patients ( n=30) was compared with non-aneurysmal tissues from organ donors ( n=31) by dot blotting and immunohistochemistry. A significantly higher expression of Hcy was observed in AAA than control tissues ( p<0.001). Furthermore, the associations of methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism, detected by polymerase chain reaction-restriction fragment length polymorphism, with both AAA and tissue Hcy expression were evaluated. Our results showed MTHFR C677T polymorphism was not significantly associated with AAA or tissue Hcy expression. Lastly, the expression of Hcy in vascular smooth muscle cells (VSMCs), which were isolated from human aortic tissues by explant culture, and their release to cultured media was investigated by dot blotting. The AAA VSMCs expressed and released a significantly higher level of Hcy than the control VSMCs ( p<0.001). In summary, our novel findings showed Hcy expression was abnormally elevated in human AAA tissues, which may not be dependent on MTHFR C677T polymorphism.
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37

Thornhill, Rosanne, Wendy Shih, Marvin I. Amen, Mohan M. John, Rosario Floridia, Anees J. Razzouk, and David G. Rabkin. "Likelihood of Aortic Valve Preservation During Repair of Acute Type A Aortic Dissection." American Surgeon 86, no. 5 (May 2020): 415–21. http://dx.doi.org/10.1177/0003134820918251.

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Background We sought risk factors for replacement of the aortic valve with or without the root (AVR/root) in the setting of acute type A aortic dissection (ATAD) repair. Methods All ATAD repairs at our institution from January 2005 to June 2018 were reviewed. Baseline characteristics were recorded. For patients with aortic valve preservation we documented the degree of aortic insufficiency (AI) postoperatively and on subsequent echocardiograms when available. Logistic regression was used to determine the association between preoperative characteristics and the odds ratio of AVR/root. Results A total of 206 patients underwent repair of ATAD. Thirty-four were excluded for no documented AI grading. Forty-six underwent AVR/root during repair of the ATAD (including 40 root replacements). Of 126 that did not undergo AVR/root, 42 (33.33%) had follow-up echocardiograms at a median of 68 months postoperatively and 2 required reintervention for valve insufficiency. Increase in degree of AI, bicuspid valve morphology, size of the aortic root, and connective tissue disorder were significantly associated with increased risk of AVR/root. Of 130 patients without connective tissue disorder, bicuspid aortic valve, aortic root aneurysm, or intimal root tear, the rate of valve preservation was 65/65 (100%), 25/29 (86.2%), and 22/40 (55%) for those presenting with mild, moderate, and severe AI, respectively. Discussion Degree of preoperative AI, bicuspid valve morphology, size of the aortic root, and connective tissue disorder significantly correlate with failure of aortic valve preservation in patients with ATAD. The vast majority of tricuspid valves in patients without connective tissue disorder or aortic root pathology can be salvaged.
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38

Torra, R., C. Nicolau, C. Badenas, C. Brú, L. Pérez, X. Estivill, and A. Darnell. "Abdominal aortic aneurysms and autosomal dominant polycystic kidney disease." Journal of the American Society of Nephrology 7, no. 11 (November 1996): 2483–86. http://dx.doi.org/10.1681/asn.v7112483.

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Although cases of autosomal dominant polycystic kidney disease (ADPKD) associated with abdominal aortic aneurysm have been repeatedly reported in the literature, no systematic studies of the aortas of these patients have been performed. In the study presented here, a sonographic study of the abdominal aorta in 139 ADPKD patients and in 149 healthy family members was carried out. For both groups, an increase in aortic diameter related to age and sex, (being wider in men than women) was found. In ADPKD patients, neither a wider aortic diameter nor a higher prevalence of abdominal aortic aneurysms could be found in any age group. It was concluded that, although these patients are prone to develop aortic aneurysms because of hypertension and associated connective tissue disorders, the presence of abdominal aortic aneurysms should be questioned as a frequent feature of ADPKD.
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39

Lee, Cheul, Jae Young Lee, and Eun-Jung Lee. "Repair of interrupted aortic arch using autologous pulmonary artery tissue." Cardiology in the Young 28, no. 3 (November 29, 2017): 464–66. http://dx.doi.org/10.1017/s1047951117002037.

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AbstractThere are several options for the repair of interrupted aortic arch. Direct anastomosis may cause several problems including anastomotic site stenosis, left main bronchus compression, and acute-angled aortic arch. Interposition of a prosthetic graft has no growth potential. We present a case of 34-month-old child with interrupted aortic arch, which was repaired using a pulmonary autograft tube.
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40

Gosline, J. M., and R. E. Shadwick. "The mechanical properties of fin whale arteries are explained by novel connective tissue designs." Journal of Experimental Biology 199, no. 4 (April 1, 1996): 985–97. http://dx.doi.org/10.1242/jeb.199.4.985.

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The aortic arch and the descending aorta in the fin whale (Balaenoptera physalus) are structurally and mechanically very different from comparable vessels in other mammals. Although the external diameter of the whale's descending thoracic aorta (approximately 12 cm) is similar to that predicted by scaling relationships for terrestrial mammals, the wall thickness:diameter ratio in the whale (0.015) is much smaller than the characteristic value for other mammals (0.05). In addition, the elastic modulus of the thoracic aorta (12 MPa at 13 kPa blood pressure) is about 30 times higher than in other mammals. In contrast, the whale's aortic arch has a wall thickness/diameter ratio (0.055) and an elastic modulus (0.4 MPa) that are essentially identical to those for other mammals. However, the aortic arch is unusual in that it can be deformed biaxially to very large strains without entering a region of high stiffness caused by the recruitment of fully extended collagen fibres. Chemical composition studies indicate that the elastin:collagen ratio is high in the aortic arch (approximately 2:1) and that this ratio falls in the thoracic (approximately 1:2) and abdominal (approximately 1:3) aortas, but the magnitude of the change in composition does not account for the dramatic difference in mechanical properties. This suggests that there are differences in the elastin and collagen fibre architecture of these vessels. The descending aorta contains dense bands of tendon-like, wavy collagen fibres that run in the plane of the arterial wall, forming a fibre-lattice that runs in parallel to the elastin lamellae and reinforces the wall, making it very stiff. The aortic arch contains a very different collagen fibre-lattice in which fibres appear to have a component of orientation that runs through the thickness of the artery wall. This suggests that the collagen fibres may be arranged in series with elastin-containing elements, a difference in tissue architecture that could account for both the lower stiffness and the extreme extensibility of the whale's aortic arch. Thus, both the structure and the mechanical behaviour of the lamellar units in the aortic arch and aorta of the whale have presumably been modified to produce the unusual mechanical and haemodynamic properties of the whale circulation.
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41

Giannini, C., M. Ladisa, V. Lutz-Bueno, A. Terzi, M. Ramella, L. Fusaro, D. Altamura, et al. "X-ray scanning microscopies of microcalcifications in abdominal aortic and popliteal artery aneurysms." IUCrJ 6, no. 2 (February 15, 2019): 267–76. http://dx.doi.org/10.1107/s2052252519001544.

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Abdominal aortic and popliteal artery aneurysms are vascular diseases which show massive degeneration, weakening of the vascular wall and loss of the vascular tissue functionality. They are driven by inflammatory, hemodynamical factors and biological alterations that may lead, in the case of an abdominal aortic aneurysm, to sudden and dangerous ruptures of the arteries. Here, human aortic and popliteal aneurysm tissues were obtained during surgical repair, and studied by synchrotron radiation X-ray scanning microdiffraction and small-angle scattering, to investigate the microcalcifications present in the tissues. Data collected during the experiments were transformed into quantitative microscopy images through the combination of statistical approaches and crystallographic methods. As a result of this multi-step analysis, microcalcifications, which are markers of the pathology, were classified in terms of chemical and structural content. This analysis helped to identify the presence of nanocrystalline hydroxyapatite and microcrystalline cholesterol, embedded in myofilament, and elastin-containing tissue with low collagen content in predominantly nanocrystalline areas. The generality of the approach allows it to be transferred to other types of tissue and other pathologies affected by microcalcifications, such as thyroid carcinoma, breast cancer, testicular microlithiasis or glioblastoma.
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42

McCabe, Michael, Sandra Toth, Doran Mix, Ibrahima Bah, Michael C. Stoner, Bruce Goldman, Mark Buckley, Scott Cameron, and Michael Richards. "Biomechanical Correlates of Tissue Architecture in Healthy and Aneurysmal Aortic Tissue." Journal of Vascular Surgery 74, no. 3 (September 2021): e294-e295. http://dx.doi.org/10.1016/j.jvs.2021.06.436.

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43

Manchenko, A., I. Mikhailova, and B. Sandomirsky. "Morphology of tissue reaction in rats after subcutaneous implantation of porcine pericardium and aortic valve leaflets devitalized by cryoradiation." Cell and Organ Transplantology 4, no. 1 (May 31, 2016): 39–46. http://dx.doi.org/10.22494/cot.v4i1.4.

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The decrease of immunogenicity is a priority requirement to pre-implantation treatment of the xenogeneic graft tissue. To create tissue implants of the pericardium and aortic valve leaflets, we have developed a method of devitalizing treatment, based on the combined effect of low temperatures (-196 °C) and ionizing β-radiation. This approach provides deletion to the main targets of biomaterial immunogenicity due to the effects of successive cryo- and radiation damage, as well as the activation of radiation-induced apoptosis.The purpose of research was to assess the impact of low-temperature and radiation and their synergistic effect on the biocompatibility of devitalized xenogeneic tissues.Methods. Histological tests were used to study tissue reaction in experimental animals after implantation of native porcine pericardium and aortic valve leaflets (control), grafts after freezing-thawing and grafts after freezing-thawing with irradiation at a dose of 25 kGy. After 7, 14 days and 1, 3, 6 and 12 months we evaluated the morphological changes of implant structure, inflammatory response of the recipient’s tissue, formation of the capsule and its degree of maturity, the xenogeneic cells survival and recovery of recipient’s surrounding tissue.Results. Comparative analysis has revealed fundamental differences of engraftment indicators and tissue reaction of cryopreserved and irradiated samples from implants after freezing and β-radiation. Cryoradiation processing greatly reduced the immune response to the implantation. Devitalized tissues promoted early stimulation of recipient’s tissues repair, maintained compactness and structural integrity. After a year the border between the implant and connective tissue erased, biomaterial was fully sprouted with recipient’s tissue. The observed changes testify to the integration of implant’s connective tissue, followed by its replacement.Conclusion. Our study has confirmed the possibility of using xenogeneic pericardium and aortic valve leaflets, being modified by cryoradiation method to restore soft tissue structures.
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Kapelouzou, Alkistis, Loukas Tsourelis, Loukas Kaklamanis, Dimitrios Degiannis, Nektarios Kogerakis, and Dennis V. Cokkinos. "Serum and tissue biomarkers in aortic stenosis." Global Cardiology Science and Practice 2015, no. 4 (September 2015): 49. http://dx.doi.org/10.5339/gcsp.2015.49.

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45

Malvindi, Pietro Giorgio, Paolo Berretta, Jacopo Alfonsi, and Marco Di Eusanio. "Tissue aortic valve replacement: expectations and reality." European Journal of Cardio-Thoracic Surgery 61, no. 4 (January 24, 2022): 897–98. http://dx.doi.org/10.1093/ejcts/ezac030.

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46

Shon, Y. H. "Proteoglycan in porcine aortic tissue after cryopreservation." Journal of Korean Medical Science 12, no. 5 (1997): 398. http://dx.doi.org/10.3346/jkms.1997.12.5.398.

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47

Al-Halees, Z. "Pulmonary artery augmentation with autologous aortic tissue." European Journal of Cardio-Thoracic Surgery 12, no. 3 (September 1997): 456–59. http://dx.doi.org/10.1016/s1010-7940(97)00189-9.

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48

Elkins, Ronald C., and Mary M. Lane. "Autologous Tissue in Complex Aortic Valve Disease." Seminars in Thoracic and Cardiovascular Surgery 13, no. 3 (July 2001): 267–72. http://dx.doi.org/10.1053/stcs.2001.22989.

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49

Yoder, Mervin C. "Aortic Tissue as a Niche for Hematopoiesis." Circulation 125, no. 4 (January 31, 2012): 565–67. http://dx.doi.org/10.1161/circulationaha.111.078865.

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50

Preventza, Ourania, and Joseph S. Coselli. "In pregnancy, aortic tissue is the issue." Journal of Thoracic and Cardiovascular Surgery 153, no. 2 (February 2017): S48—S49. http://dx.doi.org/10.1016/j.jtcvs.2016.06.050.

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